Fluid and Electrolyte
Disorders
J.B. Handler, M.D.
Physician Assistant Program
University of New England
1
Abbreviations
• ABG- arterial blood gas
• SIADH- syndrome of
inappropriate ADH
• ADH- anti-diuretic hormone
• Cr- creatinine
• AVP- arginine vasopressin
• N- nausea
• HA- headache
• OSM- osmolality
• DI- diabetes insipidus
• ACEI- angiotensin
converting enzyme inhibitor
• HTN- hypertension
• PE- physical exam
• HF- heart failure
• WNL- within normal limits
•
•
•
•
•
•
•
•
•
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•
•
•
•
BS- blood sugar
RRR- regular rate & rhythm
Mg- magnesium
AMI- acute myocardial
infarction
S04- sulfate
Ca- calcium
Nl- normal
DKA- diabetic ketoacidosis
ECF- extracellular fluid
EF- ejection fraction
MR- mitral regurgitation
MSE- mental status exam
BP- blood pressure
UT- urinary tract
2
Alterations of Fluid Volume
• Volume overload (e.g. HF): Increase in total
body fluid/Na.
– Findings: weight; edema, ascites.
• Volume depletion (vomiting, diarrhea):
– Wt. loss, excessive thirst, postural hypotension
and dry mucous membranes; both H2O and salt
are lost.
• Dehydration: Refers to volume depletion with
disproportionate water deficit; may lead to
Na, osmolality.
– Most common cause of dehydration worldwide:
diarrhea; others- heat related illness, fevers,
3
Electrolyte Values
•
•
•
•
Na
135-145 meq/L
K
3.5-5 meq/L
Cl
98-107 meq/L
HCO3 22-28 meq/L (equivalent to total
venous *CO2 done via lab testing)
• Mg
1.6-3.0 mg/dl
• Ca: total/ionized (see below)
*Total CO2 = dissolved CO2 + (H2CO3) +HCO3 (90-95% of total CO2)
Therefore, total venous CO2  HCO3
4
Renal Function
• Creatinine 0.6- 1.2 mg/dL: breakdown
product of muscle energy metabolism;
lower in women than men, reflects lean
muscle mass. Good indicator of
glomerular filtration.
• Blood Urea Nitrogen (BUN) 8-20
mg/dL- end product of protein
metabolism; excreted by kidney.
5
Clinical Implications
• May be asymptomatic
• Variety of symptoms (often neuromuscular)
depending on the electrolyte disturbance:
– Hyponatremia: weakness, delerium, seizures
– Hypokalemia: arrhythmias, muscle weakness,
cramps
– Hyperkalemia: weakness, diarrhea
– Hypocalcemia: cramps, arrhythmias, seizures
– Hypercalcemia: polyuria, constipation,
lethargy/confusion
• Measurement of electrolytes is essential in6
patients with neuromuscular symptoms
Clinical Evaluation
• History including Neuro, CV, GI, GU ROS.
• Assess neurologic status (including MSE)–
may reflect severe electrolyte imbalance,
hypoxia, hypoglycemia, etc.
• Assess volume status- weight, skin turgor,
BP, P, postural changes, mucous
membranes, edema.
• Assess metabolic and renal status –
glucose, BUN, Cr, electrolytes (Na, K, Cl,
HCO3), Ca, Mg, O2 sat.
7
Clinical Evaluation
• When indicated- serum osmolality, urine Na,
O2 sat, ABG’s (acid-base disturbance).
• Serum Osmolality: Normal 285-293 mosm/kg.
Osm = 2(Na meq/L) + Glucose mg/dl +
18
*BUN mg/dl
2.8
Represents solute [ ]: # particles in solution.
8
*Urea is an ineffective osmole; easily permeates cell membranes
Case 1
• 42 y/o female with HTN- 3 day history of
severe N&V; oral intake limited to tea and
sips of H2O.
• Meds: HCTZ 25 mg/daily; not taken in 48 hrs.
• PE: P-120, BP 90/60 lying, 70/50 upright;
weight 5 pounds in last 3 days.
• Labs: Na-125 meq/L, K-2.8 meq/L, Cl88meq/L, Cr-1.0 mg/dL, BUN-24 mg/dL,
HCO3-35 meq/L, Glu-100 mg/dL; urine Na- 5
meq/L.
• Describe the abnormal findings and why they 9
Hyponatremia
• Definition: Na< 130 meq/L
• Volume status and osmolality
essential for clarification. What
change in osmolality is most commonly
found….?
• Most cases of hypoNa result from H2O
imbalance (from ADH secretion), not
Na imbalance. The result is a relative
increase in intravascular free H2O,
leading to a dilutional decrease in Na. 10
Hyponatremia and Volume
• HypoNa can occur with hypo, hyper and
euvolemia (more examples to follow).
• When hypovolemia is present, important to
determine if basis is renal (salt wasting
nephropathy, diuretics) or non-renal (GI
losses-vomiting/diarrhea, sweating, etc.).
Urine Na is useful to differentiate renal vs
non-renal etiologies:
– If < 10 meq/L implies avid Na retention by kidney
(in absence of diuretics) non-renal loss
(vomiting, etc).
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If > 20 meq/L indicates renal salt wasting
(diuretics, salt wasting nephropathy).
ADH/AVP Secretion
• Very small increases in plasma osmolality (12%) result in ADH secretion from the
neurohypophysisosmolality & Na
maintained.
• Large changes (5-10%) in volume (with
concomitant decrease in BP) also result in
ADH release (mediated through baroreceptors in the circulation) free H2O is
retainedhypoNa.
– Marked  in CO and BP can mimic (see below)
• With hypovolemia both Na/H2O (via RAA) and12
free H O (via increased ADH/thirst) will be
Case 1
•
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•
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Volume: Decreased
Total body Na: Decreased
Serum Osmolality: Decreased
ADH secretion: Increased– why?
Renal status: preserved
Hyponatremia- why? - ADH
Hypokalemia- why? – diuretic/ALD
Predicted arterial pH- alkalotic …why?  see
lecture on Acid-Base disorders.
13
Hypovolemic Hypotonic
HypoNa
• Decreased Na with decreased ECF
volume: Renal (diuretics) or extrarenal
(vomiting, diarrhea) volume loss. Total body
Na/H2O decreased.
• ADH secretion is increased to maintain
intravascular volume. This drive overrides
the need to sustain normal osmolality. Patient
often initially unable to take in adequate
Na/H2O orally.
• Rx (Case 1): Isotonic fluids IV (normal
saline/0.9% saline or ringers lactate) with
KCL. If mild volume  and oral intake intact:
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Electrolyte drink (“Gatorade”) + KCL.
Case 2
• 55 y/o man with dilated cardiomyopathy (EF
24%) presents with recurrent shortness of
breath, wt gain and leg edema.
• Meds: Furosemide, metolazone*, metoprolol,
lisinopril & digoxin.
• PE: BP 88/60, Lungs- diffuse crackles; HeartS3 gallop and MR murmur; Ext- 3+ edema.
• Labs: Na-125 meq/L, K-2.9 meq/L, Cl-100
meq/L, glu- 100mg/dL, Cr-1.5 mg/dL, BUN60 mg/dL.
15
• What is going on? Management?
*thiazide like diuretic used in addition to a loop diuretic for severe HF
Case 2
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•
•
•
•
Volume: Increased
Total body Na: Increased
Serum Osmolality: Decreased
ADH secretion: Increased- why?
Renal status: Pre-renal azotemia from
renal perfusion
• Hyponatremia- why?
• Hypokalemia- why?
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Hypervolemic Hypotonic HypoNa
• Hyponatremia with increased ECF; edema
related disorders (HF, cirrhosis, nephrotic
syndrome).
• Total body Na/H2O are increased but
circulating blood volume is sensed as
inadequate by baroreceptors because of
CO and BP; CO renal perfusion (can
lead to pre-renal azotemia).
Result: Increased ADH + activation of RAA
system.
• Treatment: Water restriction, diuretics, and 17
treatment of the underlying condition (very
Case 3
• A 55 y/o man with small cell lung cancer
presents to the ED following a grand-mal
seizure. He has been treated with
chemotherapy.
• PE: P-80, BP-140/80; membranes moist, skin
turgor intact; Lungs-clear, Heart-RRR, no
murmurs; extremities- no edema, intact
pulses.
• Labs: Na- 116 meq/L, K-4.8 meq/L, Bun 8
mg/dL, Creatinine 0.9meq/L, Glu 100mg/dL.
Urine Na-36 meq/L; urine osmolality .
18
• What is going on? Management?
Case 3
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•
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Volume: Euvolemic
Total body Na: Normal
Serum Osmolality: Decreased
ADH secretion: Increased- why?
Renal status: Normal
Hyponatremia- why?
Increased urine osmolality- why?
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Euvolemic Hypotonic
Hyponatremia
• Need urine Na and osmolality to diagnose
• SIADH is most common cause. Patient is
euvolemic with inappropriate ADH
secretion.
• Etiology: Disorders of CNS (stroke), tumors
(lung Ca, others), pulmonary lesions (TB),
drugs with ADH-like effects (SSRIs, others),
post-op pain, etc.
• Hyponatremia, decreased serum osmolality
(<280 mosm/kg), with inappropriately high
urine osmolality (>150 mosm/kg).
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SIADH
• Absence of cardiac, liver, renal, adrenal or
thyroid disease.
• Urine Na >20meq/L. Natriuresis (RAAS
turned off) compensates for slight increase in
volume from ADH.
• Serum BUN and uric acid are low due to
increased clearance (mild volume
expansion).
21
Treatment of SIADH (IO)
• Symptomatic hyponatremia (Na< 120
meq/L) is a medical emergency.
• Na correction must be done slowly (<10-12
meq/L/d). Too rapid correction Central
Pontine Myelinosisirreversible and
disastrous.
• Hypertonic (3%- 513 meq/L) saline used only
for most severe cases. Must monitor serum
Na every 2 hrs and Na by no more than 1012 meq/L/d.
• Asymptomatic hyponatremia: H2O restriction
or Demeclocyline- inhibits effect of ADH on 22
IO- interest only
distal tubule.
Psychogenic Polydipsia
• Marked excess free H2O intake >10 L/d or
more.
• Seen in patients with psychiatric disease who
may be on psychiatric meds (SSRI’s, others)
that can interfere with H2O excretion.
• Euvolemia maintained via renal excretion of
H2O and Na (urine Na > 20 meq/L).
• Serum ADH levels are low.
• Urine osmolality is low.
23
Post-op Hyponatremia
• Post-op pain increases ADH secretion.
If patient receives inappropriate
administration of hypotonic fluids, result
can be severe symptomatic
hyponatremia (N, HA, seizures, etc.).
• Treatment: Appropriate pain control with
administration of isotonic fluids until
patient able to take adequate fluids
orally.
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Hypertonic Hyponatremia
• Seen with significant hyperglycemia in
diabetics, especially if insulin dependent with
an acute rise in BS osmolality. Water is
drawn from cells into extracellular space
resulting in dilution of Na.
• Na falls 2-3 meq/l for every 100mg/dL rise in
glucose above 200mg/dL; resolves with
insulin infusion and volume expansion.
• A dilutional hyponatremia. Example
covered during Acid-Base section.
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Hyponatremia and HIV/AIDS
• Common; 20% ambulatory and 50%
hospitalized patients with AIDS have
Na.
• Pathophysiology: multiple mechanisms
involved often a combination of GI fluid
and electrolyte loss along with
inappropriate ADH secretion associated
with CNS and/or pulmonary involvement
from HIV infection.
26
Hypernatremia with Concentrated
Urine
• Unusual with intact thirst mechanism and
access to H2O. “Stranded in the desert.”
• Appropriate H2O intake not possible (no H2O
available or unconscious).
• Signs/Sx: Orthostatic hypotension,
dehydration; oliguria.
• Lab: Uosm >400mosm/kg with intact renal
function. ADH levels increased.
• Non-renal H2O losses: e.g. water ingestion
fails to keep up with hypotonic losses from 27
excessive sweating, losses from GI or
Treatment of Hypernatremia
• Correct cause of fluid loss and replace
volume, water and electrolytes as
indicated.
• Replace water deficit slowly to avoid
cerebral edema (brain cell adaptation to
serum hyperosmolality). Fluid deficit
should be replaced over 48-72 hours.
• Type of fluid replacement will vary
depending on patient volume status
(0.9% saline followed by 0.45% saline).28
Case 4
• A 28 y/o woman presents to the ED with
marked dizzyness and a syncopal episode.
Marked thirst/polydipsea and urination x 1
week, nauseated without fluid intake the last
24 hours.
• Meds: started on Lithium for bipolar disease
one week ago.
• PE: P-115, B.P lying 90/60, standing 70/50;
Skin turgor  and mucus membranes dry.
• Na-150 meq/L, K-3.4 meq/L, BUN-40
meq/L, Cr-1.3meq/L.
• Urine Osm 100 mosm/kg.
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• What is going on? Management?
Hypernatremia with Dilute
Urine
• Diabetes Insipidus: thirst, H2O
(polydipsia)
• Urine osmolality < 250 mosm/kg.
• Central Diabetis Insipidus: Lack of
ADH/AVP production by posterior pituitary.
Hypernatremia due to free water loss. Rx is
with ADH.
• Nephrogenic DI (Acquired): Renal
insensitivity to ADH seen after relief of
prolonged UT obstruction; renal interstitial
disease; hypercalcemia; lithium or
demeclocycline Rx.  response to ADH.
30
Case 5
• 44 y/o man with dilated cardiomyopathy presents with
syncopal episode and weakness following 3 day
history of fever and diarrhea.
• Meds: Digoxin, lisinopril, furosemide & carvedilol.
• PE: P-105 (irregular with pauses), BP- 95/70; skin
turgor, dry mucus membranes; Heart- Tachycardic
with “extra sounds” and pauses, S3 gallop.
• Na-135 meq/L, K-2.8 meq/L, Cl-104 meq/L, HCO322meq/L; Digoxin level 2.2 ng/mL (0.8-2 ng/ml);
BUN and CR- WNL; ECG- see below
• What is going on? Other labs needed? Treatment?
31
Hypokalemia
• K is the major intracellular ion (95% IC)
• K regulation:
1. Shifts intra/extracellular
2 Renal K modulation (RAA System)
(most important)
• K uptake by cells stimulated by insulin in the
presence of glucose and facilitated by beta
adrenergic stimulation.
• Symptoms/signs: weakness, muscle cramps,
fatigue, constipation.
32
• *NSST-TECG: NSST-T*
changes
waves;
non-specific
ST and Tand
wave“U”
changes
Pathophysiology of
Hypokalemia
• Extrarenal K losses: GI via vomiting,
diarrhea.
• Renal K losses: Aldosterone facilitates urinary
K excretion; most important regulator of body
K content. Most diuretics lead to renal K
losses.
• Treatment: Mild to moderate K losses can be
replaced with oral KCL.
Severe hypokalemia requires IV
administration slowly, with cardiac
monitoring.
33
• Case 5: Hospitalize, IV fluids/KCL, frequent
Case 6
• 32 y/o man presents to the ED with 7 days of
weakness and malaise. In last 24 hours he has
become lethargic and developed diarrhea; poor
historian. No prior medical problems; no meds.
• PE: Ill appearing man, moaning. T-38.8, P-125, BP90/60; lungs- basilar crackles; heart- tachycardic
without murmur; ext-2+ edema.
• ECG done in ED (see below)- wide QRS
tachycardia, ?Vtach.
• Labs: pending; O2 sat-94% on room air.
• Cardiology consultation requested- Handler called.
34
Case 6, continued
• Cardiology consult: “I don’t think this is Vtach.
The rate slows during carotid message. Is the
potassium level back?” (ED doc skeptical).
• Labs: Na-136 meq/L, K-8.1meq/L*, Cl98meq/L, HCO3-17meq/L, BUN-90meq/L,
Cr-8.6meq/L
CxR: normal size heart; pulmonary
congestion.
• ABG- pH-7.32, PCO2-32mmHg, PO2-68
mmHg on room air. Describe acid-base
status?
*Test
repeated with same result; no hemolysis
35
• What is going on? Management?
Hyperkalemia
• Important to confirm lab values (hemolysis)
• Patients with renal insufficiency are at
risk.
• Mild K may accompany metabolic acidosis
due to intra/extra cellular shifts (H/K
exchange).
• Risk factors for developing hyperkalemia:
– Severe renal insufficiency
– Renal insufficiency plus K supplements (KCL), K
sparing diuretic or ACEI
– Combination of KCL + K sparing diuretic as Rx of 36
hypokalemia: avoid for most patients
Clinical Findings
• Abnormalities in neuromuscular
function: weakness, diarrhea, rarely
paralysis.
• Characteristic ECG findings may occur:
Peaked T waves, widening of QRS,
increased intervals, loss of p waves,
etc.
• Important to assess renal function.
37
Case 6
• Diagnosis- acute renal failure, uncertain
etiology.
• Severe hyperkalemia, secondary to renal
shutdown; acidosis also contributes.
• Compensated metabolic acidosis
secondary to uremia- to be discussed during
Acid-Base lecture.
• Infusion of Insulin/Glucose started; albuterol
by nebulizer given.
• Nephrologist called, dialysis catheter placed
38
at her request.
Treatment of Hyperkalemia
• In life threatening situations (K>6.6-7.0) an
infusion of insulin and glucose will drive K
intracellularly, buying time for further Rx. This
is potentiated by ß-agonists (albuterol).
• Eliminate K supplements/K sparing drugs
• Cation exchange resins orally or rectally
exchange Na for K (Kayexelate). Give
cautiously in HF.
• Dialysis required with severe renal failure
39
ECG: Hyperkalemia
Images.google.com
Calcium Metabolism
• 1% total body calcium is in solution in body
fluid
50% is ionized muscle & nerve function
40% is protein bound (primarily albumin)
10% complexed with anions (citrate, etc)
• Normal Total Serum Ca is 9-10.3mg/dL
Ionized Ca is 4.7-5.3 mg/dL
• Important to measure serum albumin to
determine if Ca levels reflect true
deficiency.
– For every 1 gram of albumin, total Ca s by
41
0.8meq/L. Ionized Ca is not effected by albumin
Hypocalcemia
• Most common cause is chronic renal failure
(decreased Vit D3 and increased PO4).
– Hypoparathyroidism and malabsorbtion less
common
• Signs/Sx: Increased excitation of nerve and
muscle cells; cramps, tetany, paresthesias
and convulsions.
• Chvostek’s sign, Trousseau’s sign
• ECG: Prolonged Q-T interval/arrhythmias
• Serum Ca <9.0mg/dL (nl albumin), ionized
Ca <4.5mg/dL
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Treatment: Hypocalcemia
• If symptomatic: IV calcium gluconate via
bolus and infusion.
• If asymptomatic: Oral calcium and
Vitamin D.
• Correction of hypomagnesemia if
present.
43
Hypercalcemia
• Etiologies include hyperparathyroidism,
malignancy (tumors produce PTH related
proteins), milk-alkali syndrome (Ca antacids +
Vit D excess).
• Signs/Sx: Often without sx if mild Ca
– Renal/GI: polyuria (H2O* reabsorption is
blocked by hypercalciuria), nephrolithiasis;
nausea, constipation.
– Neuro changes (drowsiness, weakness, lethargy,
stupor/coma) with severe hypercalcemia.
• ECG findings: Shortened Q-T, PVC’s.
• Lab: increased Ca with nl. or low PO4.
*Sounds like?
44
Treatment or Hypercalcemia
• Treat underlying disease process.
• Promote Na rich diuresis which will be
accompanied by excretion of Ca.
• Infusion of 0.9% Saline + IV furosemide
will expand ECF volume and promote
Na/Calcium rich diuresis.
• Avoid Thiazide diuretics: Can worsen
hypercalcemia.
45
Hypomagnesemia
• Very common in hospitalized patients,
especially those on diuretics who are
receiving continuous IV fluid support.
• Normal Mg Level: 1.5-2.5 meq/L
• Symptoms similar to hypocalcemia:
weakness, muscle cramps, tremors,
neurmuscular and CNS hyperirritability.
• Often associated with hyopK and hypoCa
• Low Mg potentiates dangerous
(ventricular) cardiac arrhythmias, esp if K
46
is low.
Treatment of
Hypomagnesemia
• Important to order Mg levels in
hospitalized cardiac patients (AMI, CHF,
etc.).
• IV therapy with MgSO4, and monitor
levels.
• Oral Mg oxide can be given for
supplemental oral use.
47